HCSGD entry for RPS6KA3
1. General information
Official gene symbol | RPS6KA3 |
---|---|
Entrez ID | 6197 |
Gene full name | ribosomal protein S6 kinase, 90kDa, polypeptide 3 |
Other gene symbols | CLS HU-3 ISPK-1 MAPKAPK1B MRX19 RSK RSK2 S6K-alpha3 p90-RSK2 pp90RSK2 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network

This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0000287 | Magnesium ion binding | IEA | molecular_function |
GO:0001501 | Skeletal system development | TAS | biological_process |
GO:0002224 | Toll-like receptor signaling pathway | IEA ISS TAS | biological_process |
GO:0002755 | MyD88-dependent toll-like receptor signaling pathway | TAS | biological_process |
GO:0002756 | MyD88-independent toll-like receptor signaling pathway | TAS | biological_process |
GO:0004672 | Protein kinase activity | TAS | molecular_function |
GO:0004674 | Protein serine/threonine kinase activity | IEA | molecular_function |
GO:0005524 | ATP binding | IEA | molecular_function |
GO:0005654 | Nucleoplasm | TAS | cellular_component |
GO:0005829 | Cytosol | TAS | cellular_component |
GO:0005840 | Ribosome | IEA | cellular_component |
GO:0007049 | Cell cycle | IEA | biological_process |
GO:0007165 | Signal transduction | TAS | biological_process |
GO:0007268 | Synaptic transmission | TAS | biological_process |
GO:0007411 | Axon guidance | TAS | biological_process |
GO:0007417 | Central nervous system development | TAS | biological_process |
GO:0019901 | Protein kinase binding | IEA | molecular_function |
GO:0030307 | Positive regulation of cell growth | TAS | biological_process |
GO:0032496 | Response to lipopolysaccharide | IEA ISS | biological_process |
GO:0034134 | Toll-like receptor 2 signaling pathway | TAS | biological_process |
GO:0034138 | Toll-like receptor 3 signaling pathway | TAS | biological_process |
GO:0034142 | Toll-like receptor 4 signaling pathway | TAS | biological_process |
GO:0034146 | Toll-like receptor 5 signaling pathway | TAS | biological_process |
GO:0034162 | Toll-like receptor 9 signaling pathway | TAS | biological_process |
GO:0034166 | Toll-like receptor 10 signaling pathway | TAS | biological_process |
GO:0035666 | TRIF-dependent toll-like receptor signaling pathway | TAS | biological_process |
GO:0038123 | Toll-like receptor TLR1:TLR2 signaling pathway | TAS | biological_process |
GO:0038124 | Toll-like receptor TLR6:TLR2 signaling pathway | TAS | biological_process |
GO:0043027 | Cysteine-type endopeptidase inhibitor activity involved in apoptotic process | IDA | molecular_function |
GO:0043066 | Negative regulation of apoptotic process | TAS | biological_process |
GO:0043154 | Negative regulation of cysteine-type endopeptidase activity involved in apoptotic process | IDA | biological_process |
GO:0043555 | Regulation of translation in response to stress | TAS | biological_process |
GO:0043620 | Regulation of DNA-templated transcription in response to stress | TAS | biological_process |
GO:0045087 | Innate immune response | TAS | biological_process |
GO:0045597 | Positive regulation of cell differentiation | TAS | biological_process |
GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IMP | biological_process |
GO:0048011 | Neurotrophin TRK receptor signaling pathway | TAS | biological_process |
GO:0051403 | Stress-activated MAPK cascade | TAS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.0073629421 | 0.5862509973 | 0.2247319444 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Up | 0.1432424869 |
GSE13712_SHEAR | Down | -0.0315552754 |
GSE13712_STATIC | Down | -0.1008102548 |
GSE19018 | Down | -0.8181564115 |
GSE19899_A1 | Up | 1.0619107043 |
GSE19899_A2 | Up | 0.8108887960 |
PubMed_21979375_A1 | Up | 1.8746017248 |
PubMed_21979375_A2 | Up | 1.3822488221 |
GSE35957 | Up | 0.1312367886 |
GSE36640 | Down | -0.0968383230 |
GSE54402 | Up | 1.1608371818 |
GSE9593 | Up | 0.0187230526 |
GSE43922 | Up | 0.7830018285 |
GSE24585 | Down | -0.5913315034 |
GSE37065 | Up | 0.2790195543 |
GSE28863_A1 | Up | 0.6196553208 |
GSE28863_A2 | Up | 0.4135484511 |
GSE28863_A3 | Down | -0.7277176819 |
GSE28863_A4 | Up | 0.1166762736 |
GSE48662 | Down | -0.1033013458 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Name | Drug | Accession number |
---|---|---|
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-21-5p | MIMAT0000076 | MIRT030861 | Microarray | Functional MTI (Weak) | 18591254 |
hsa-miR-16-5p | MIMAT0000069 | MIRT031564 | Microarray | Functional MTI (Weak) | 21199864 |
hsa-miR-1296-5p | MIMAT0005794 | MIRT036103 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-503-5p | MIMAT0002874 | MIRT041136 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-320a | MIMAT0000510 | MIRT044599 | CLASH | Functional MTI (Weak) | 23622248 |
hsa-miR-29a-3p | MIMAT0000086 | MIRT049971 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 5 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
27125759 | We have compared results from published genome-wide, chronological lifespan (CLS) screens of individual gene deletion strains in Saccharomyces cerevisiae in order to identify gene deletion strains with consistent influences on longevity as possible indicators of fundamental aging processes from this single-celled, eukaryotic model organism |
27125759 | We performed a comparison among the data sets using correlation and decile distribution analysis to describe concordance between screens and identify strains that consistently increased or decreased CLS |
27125759 | We attempted to replicate the different experimental conditions employed by the screens to identify potential sources of variability in CLS worth further investigating |
27125759 | To test the hypothesis that different parental strain auxotrophic requirements or media formulations employed by the respective genome-wide screens might contribute to the lack of concordance, different CLS assay conditions were assessed in combination with strains having different ploidy and auxotrophic requirements (all relevant to differences in the way the three genome-wide CLS screens were performed) |
27125759 | This limited but systematic analysis of CLS with respect to auxotrophy, ploidy, and media revealed several instances of gene-nutrient interaction |
27125759 | CONCLUSIONS: There is surprisingly little overlap between the results of three independently performed genome-wide screens of CLS in S |
27125759 | Considering the lack of overlap in CLS phenotypes among the set of genes reported by all three screens, and the results of a CLS experiment that systematically tested (incorporating extensive controls) for interactions between variables existing between the screens, we propose that discrepancies can be reconciled through deeper understanding of the influence of cell intrinsic factors such as auxotrophic requirements ploidy status, extrinsic factors such as media composition and aeration, as well as interactions that may occur between them, for example as a result of different pooling vs |
27125759 | Such factors may have a more significant impact on CLS outcomes than previously realized |
27125759 | Future studies that systematically account for these contextual factors, and can thus clarify the interactions between genetic and nutrient factors that alter CLS phenotypes, should aid more complete understanding of the underlying biology so that genetic principles of CLS in yeast can be extrapolated to differential cellular aging observed in animal models |
25452419 | Chronological lifespan (CLS) has been studied in stationary-phase yeast cells depleted for glucose, which only survive for a few days |
25452419 | Here, we analyzed CLS in quiescent S |
25452419 | We independently verified the extended CLS in individual assays for 30 selected mutants, showing the efficacy of the screen |
25452419 | Unlike for stationary-phase cells, no inverse correlation between growth and CLS of quiescent cells was evident |
24841311 | Chronological life-span (CLS) measures the length of time nondividing cells survive |
24841311 | Here, we describe methods used to measure yeast RLS and CLS |
21736893 | Yeast chronological life span (CLS) is defined as the capacity of stationary cultures to maintain viability over time, thus mimicking the situation of post-mitotic cells in multicellular organisms |
21736893 | This study describes the optimization and validation of a method based on the flow cytometric monitoring of propidium iodide (PI) uptake for assessing yeast cell death during CLS |
21736893 | The method was validated by determining CLS of several strains used in yeast ageing research and by evaluating the effect of genetic disturbances known to extend or reduce yeast chronological life span |
19306530 | Furthermore, a detailed atlas of fat depot-specific differences in adipocyte size and CLS prevalence has begun in two genetic models of mouse obesity |
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